Role of Gynecologic Findings in Interstitial Cystitis/Bladder Pain Syndrome: A Consensus

A number of associated gynecologic disorders overlap with IC/BPS, our consensus committee identified five main co‐morbid disorders: 1. Endometriosis/Adenomyosis 2. Vulvodynia/Vestibulodynia 3. Sexual Dysfunction/Genito‐Pelvic Pain/Penetration Disorder 4. Overactive Pelvic Floor Muscles 5. Hormone‐ Associated Genitourinary Changes Endometriosis/Adenomyosis Vulvodynia/Vestibulodynia Sexual Dysfunction/Genito‐Pelvic Pain/Penetration Disorder Overactive Pelvic Floor Muscles Hormone‐ Associated Genitourinary Changes Endometriosis is characterized by the presence of endometrial‐like tissue (‘lesions’) outside of the uterus and is considered a chronic, estrogen dependent, inflammatory condition. Presenting symptoms may include a variety of often debilitating pelvic pain symptoms and infertility. However, many women with endometriosis have no symptoms at all. Endometriotic lesions can be found throughout the pelvis, including in the bladder and on the overlying peritoneum. It is important to note that pain symptoms do not correlate with either the location or severity of disease [ 6 ]. Several theories attempt to explain the etiology of endometriosis, including retrograde menstruation, hematogenous or lymphatic transport, and intraperitoneal metaplasia [ 7 ]. There is certainly a genetic component, and it is interesting to note that there is a shared genetic contribution to endometriosis and both other pain and inflammatory conditions [ 8 ]. Traditional views of endometriosis‐associated pain attributed the symptoms to the lesions and associated inflammation and fibrosis. There is evidence that inflammatory mediators play a role, and this may be particularly important in generating dysmenorrhea. However, more recent work has highlighted the complexity of the mechanisms underlying endometriosis‐associated pain and demonstrated the presence of non‐nociceptive mechanisms (both neuropathic and nociplastic components) for a significant proportion of women. Many of the mechanisms associated with endometriosis‐associated pain have also been described for IC/BPS [ 9 , 10 ]. It is well established that endometriosis and IC/BPS frequently co‐exist. Prospective studies have reported an overlap between the two conditions in approximately 65% of patients [ 11 , 12 ]. IC/BPS patients with endometriosis tend to have a large bladder capacity, increased incidence of chronic fatigue, fibromyalgia, migraines, and pelvic floor dysfunction consistent with the systemic phenotype of IC/BPS [ 13 ]. Patients with IC/BPS often describe similar symptoms to those with endometriosis and thus “classic” endometriosis symptoms of dysmenorrhea or dyspareunia are not sufficient to distinguish between diagnoses [ 14 ]. Whenever endometriosis lesions are present within the bladder, it may be appropriate to attribute symptoms to these lesions. However, given that many women with endometriosis and bladder symptoms do not have bladder lesions, endometriosis per se should not be an exclusion to the diagnosis of IC/BPS. Where bladder symptoms do not improve with standard endometriosis treatments (hormonal or surgical) a diagnosis of comorbid IC/BPS would be appropriate. Adenomyosis is a condition related to endometriosis, where endometrial‐like tissue is found within the myometrial layer of the uterus. Until recently, its diagnosis was histology‐based on hysterectomy specimens and thus was considered a disease of later reproductive age. However, advanced ultrasound and MRI imaging has allowed improvement in clinical diagnosis, leading to increased awareness of its occurrence in young women as well. Adenomyosis is commonly comorbid with endometriosis and may be responsible for symptoms previously attributed to endometriosis. It is likely that many of the etiological factors are similar between the two conditions [ 15 , 16 ]. Given the location of the adenomyotic tissue in the uterus itself and lack of direct bladder involvement, this condition does not represent a possible differential diagnosis for IC/BPS. However, it may well be a contributing factor in the development of IC/BPS, given its association with inflammation and visceral hyperalgesia. Dysmenorrhea is a particularly common symptom of adenomyosis and it is notable that those with dysmenorrhea (whether or not associated with pathology) often exhibit “silent” bladder symptoms that may precede the development of more obvious symptomatology [ 17 ]. The most recent consensus from the International Society for the Study of Vulvovaginal Disease, the International Society for the Study of Women's Sexual Health, and the International Pelvic Pain Society defines vulvar pain (also known as ‘vulvodynia’) as a condition lasting ≥ 3 months without another identifiable cause. Vulvar pain can be localized (e.g., vestibulodynia, clitorodynia) or generalized, and may be provoked (e.g., during tampon insertion, sexual activity, speculum examination, or other contact) or spontaneous [ 18 ]. Vulvodynia is a multifactorial condition, with potential etiologies including hormonal influences (e.g., contraceptives), genetic factors, inflammation, musculoskeletal issues (e.g., overactive pelvic floor), central or peripheral (neuroproliferation) neuropathic mechanisms, psychosocial factors (e.g., anxiety, depression, PTSD), and structural abnormalities (e.g., pelvic organ prolapse) [ 18 ]. In addition to IC/BPS, vulvodynia often co‐occurs with other chronic pain conditions, such as fibromyalgia, irritable bowel syndrome (IBS), and temporomandibular disorder. Among patients with IC/BPS, the prevalence of concurrent vulvodynia diagnoses ranges from 25% to 85% [ 19 , 20 , 21 ]. A recent study compared 37 IC/BPS patients vs controls, observing worse vulvodynia swab test and poor vaginal health in the study group [ 22 ]. Embryologically, the urogenital sinus gives rise to the urethra, bladder, distal vagina, and vestibule, suggesting that a disorder of urogenital sinus‐derived epithelium could lead to concurrent pain in both the vestibule and the bladder [ 20 , 23 ]. Provoked Vestibulodynia (PVD), a specific form of provoked vestibular pain, has been associated with increased mast cell activity, observed through immunohistochemical staining of tissue samples following vestibulectomy. Notably, 61% of individuals with PVD report at least one comorbid condition linked to mast cell activation [ 24 ]. This aligns with the overlap with IC/BPS, where abnormal mast cell activation and neuropathic pain are common [ 25 ]. Mast cells trigger histamine release resulting in hyperalgesia and neuropathic pain, forming a “wind‐up” cycle wherein repeated activation of nociceptive pathways exacerbates pain sensitivity [ 10 , 23 ]. This mechanism can extend beyond the bladder, affecting the peritoneum (e.g., endometriosis), bowel (e.g., irritable bowel syndrome), and vulvar/vaginal regions (e.g., vulvodynia). Allodynia occurs when non‐painful stimuli are perceived as painful, due to upregulation of sensory information and subsequent hyperalgesia [ 10 , 23 , 25 ]. Female Sexual Dysfunction (FSD) is common across all age groups and is particularly prevalent in women with IC/BPS. The Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network found decreased sexual function and satisfaction in both sexes with IC/BPS [ 26 ]. FSD is categorized into four domains: hypoactive sexual desire dysfunction (HSDD), female sexual arousal dysfunction (FSAD), female orgasmic dysfunction (FOD) and GPPPD [ 27 ]. The ICSM definition of Genito‐Pelvic Pain/Penetration Disorder (GPPPD) includes persistent or recurrent difficulties with at least one of the following: (i) vaginal penetration during intercourse; (ii) marked vulvovaginal or pelvic pain during genital contact; (iii) marked fear or anxiety about vulvovaginal or pelvic pain in anticipation of, during, or as a result of genital contact; or (iv) marked hypertonicity or overactivity of pelvic floor muscles with or without genital contact [ 27 ]. This classification mirrors the DSM‐5 merging of vaginismus and dyspareunia (which consisted two separate diagnoses in the DSM‐IV), driven by the significant overlap and widespread co‐morbidity of these conditions. In the context of IC/BPS, the pathophysiology of sexual pain may be related to all elements mentioned in the definition of GPPPD. The available evidence on the association of IC/BPS with specific FSD domains is regrettably very scant. Sacco et al found that among 191 women with LUTS, those with IC/BPS had the highest FSD rates (46.1%), with domain‐specific rates of 58.3% for HSDD, 38.9% FSAD, 47.2% FOD, and 83.3% GPPPD [ 28 ]. In a larger survey of 985 women with IC/BPS, 88% with a sexual partner reported one FSD symptom, and 90% reported an IC/BPS‐specific FSD symptom in the past month [ 29 ]. A case‐control study comparing 215 women with IC/BPS to 832 controls showed reduced sexual desire and orgasm, and significantly higher sexual distress (18.5 ± 14.3 vs. 8.3 ± 10.2, p  < 0.001) [ 30 ]. As opposed to the paucity of data on desire, arousal and orgasm, sexual pain in women with IC/BPS is well documented [ 31 ]. Up to 75% of women with IC/BPS report that sexual activity worsens their symptoms [ 25 ]. Pain during intercourse is a major reason for sexual avoidance [ 21 , 32 ]. The aforementioned case‐control study also found significantly more dyspareunia (75% vs. 30%) and fear of pain (50% vs. 13%) in IC/BPS patients [ 30 ]. Clinical evidence indicates considerable symptom overlap between GPPPD and IC/BPS, often creating a vicious cycle that exacerbates both conditions. In women with IC/BPS and overlapping vulvodynia, these conditions can severely impact sexual health and overall well‐being [ 21 ]. Similarly, women with comorbid endometriosis and IC/BPS reported significantly greater pain intensity during intercourse than those with either condition alone, and greater postcoital pain than those with endometriosis alone [ 14 ]. Despite evidence from clinical studies, preclinical studies have regrettably overlooked the relationship between IC/BPS and dyspareunia: future models in rodents should take care to fill this gap [ 33 ]. The IUGA/ICS joint report on female pelvic floor dysfunction adopted the term “overactive pelvic floor muscles” to encompass various forms of dysfunction, including high‐tone pelvic floor, non‐relaxing pelvic floor, fixed pelvic floor, and pelvic floor tenderness. Overactive pelvic floor muscles can result from a pain cycle and/or a guarding response. This dysfunctional muscle engagement is typically involuntary, leading to an inability to relax the pelvic floor, which can cause difficulty during micturition or defecation [ 34 ]. The overlap between OPF and IC/BPS is considerable, with as many as 85% of patients with IC/BPS diagnosed with overactive pelvic floor muscles or levator ani pain [ 25 , 35 ]. A recent study of 92 IC/BPS patients reported 85.8% had pelvic floor myalgia, which was associated with higher IC symptom scores but not with bladder capacity, glomerulation, bladder wall thickness, or urine biomarkers [ 36 ]. The latter data provide further evidence on the complexity of the intersection of IC/BPS and OPF, often influenced by a combination of anxiety, trauma, injury, surgery, and lifestyle factors [ 37 , 38 ]. This multimodal process requires careful attention to both physical and psychological components of pelvic pain. The diagnosis of overactive pelvic floor (OPF) may be confirmed during a vaginal exam, where the clinician palpates taut muscles or patient perceived tenderness in the pelvic floor muscles (PFM), such as the levator ani, obturator internus, piriformis, or coccygeus [ 2 , 34 , 39 ]. Meister et al. developed a standardized and reproducible pelvic floor muscle examination protocol to help clinicians diagnose and assess the severity of overactive pelvic floor dysfunction in women [ 40 ]. Symptoms and signs include: pelvic or bladder pain, bladder storage and voiding symptoms, GPPPD, defecatory dysfunction, abnormal muscle function (trigger points), and pudendal nerve distribution pain [ 39 , 41 , 42 ]. From a biomedical perspective, OPF may be the result of altered voluntary activation or reflex control. A small comparative study on 15 women with IC/BPS vs 15 healthy controls observed significantly higher PFM resting EMG activity in the study group, along with shortened PFM in 80% of women [ 43 ]. Moreover, the increased PFM activity correlated with reported pain. From a bio‐psychosocial perspective, OPF may reflect anxiety, or a learned guarding response to experiences involving not only chronic pain but also fear of pain or trauma [ 42 ]. Traumatic sexual experiences, in particular, have been shown to increase the odds of developing bladder pain, suggesting that a stressful inflammatory state or psychiatric component may exacerbate pain perception [ 44 ]. In a cross‐sectional case‐control survey, Peters et al. identified a higher rate of past abuse (37% vs 22%, p  < 0.001) and of sexual abuse (SA) (17.7% vs 8.2%, p  < 0.001) in participants with IC/BPS vs comparisons [ 35 ]. In an additional cross‐sectional study comparing 207 IC/BPS patients to 117 controls, participants with IC/BPS reported a higher rate of past rape/sexual molestation as compared to comparisons (24% vs 14.7%, p  = 0.047) [ 45 ]. Furthermore, participants with past SA presented with higher pain levels, more depression, and poorer quality of life. Childhood trauma, particularly involving close family members, has also been identified as a risk factor for a psychosocial phenotype of IC/BPS, which emphasizes the need for a more comprehensive approach to treatment [ 46 ] and a broader approach to discussions of trauma/adverse events rather than focusing solely on those of a sexual nature. In a large longitudinal cohort of female and male UCPPS patients, Naliboff et al. observed higher level of lifetime and current stress in the study group vs comparisons [ 26 ]. Psychosocial factors should be considered when evaluating patients with IC/BPS, particularly when identifying different disease phenotypes. In a small but interesting retrospective case‐control study of 119 women with newly diagnosed IC/BPS, the authors observed significant differences between 30 women with a SA history and 89 women with no such history [ 47 ]. Participants with the SA history presented with less increased daytime frequency and nocturia, larger voided volumes, greater tenderness upon pelvic exam, and lower sexual function scores in all domains of the Female Sexual Function Index. These findings, indicating better preserved bladder function along with greater chronic pain and poorer sexual function in the group with past SA, may indicate two distinct clinical presentations of bladder‐centered versus non‐bladder‐centered disease, which may help guide a psychosocial multimodal approach to treatment. The pain associated with GPPPD, which can overlap with generalized, unprovoked vulvodynia, often triggers a reflexive muscle tension as the body attempts to shield itself from perceived pain. However, when this muscle tension becomes chronic, such as in OPF, it perpetuates the pain cycle, creating a vicious feedback loop where pain and muscle tightness intensify each other. This results in a complex and challenging clinical scenario, where it can be difficult to distinguish whether the pain originates from the muscles, the bladder, both or another underlying condition, further complicating diagnosis and treatment. In summary, the presence of OPF does not exclude a diagnosis of IC/BPS but would highlight the need for a multi‐disciplinary treatment approach for optimum symptom management. The association with trauma and with behavioral responses should prompt input from clinical psychologists as well as physical therapists. Hormonal factors—including menstrual cycle variation, pregnancy, menopause, and changes from exogenous hormone use (e.g., contraception, endometriosis treatment, or hormone replacement therapy)—can all influence pelvic pain. IC/BPS symptoms often fluctuate with the menstrual cycle, with many women reporting increased pain in the week before menses [ 25 , 48 ]. Clinicaly, this pattern could suggest possible overlap with conditions like endometriosis or adenomyosis, which also worsen during menstruation, but may also be due to hormonal influences on other pelvic organs and components of the pain neuroaxis [ 2 , 9 , 48 ] Urodynamic studies show that women with IC/BPS may experience increased pain at lower bladder volumes during the follicular phase compared to the luteal phase [ 48 ]. Hormonal fluctuations play a significant role in the pathophysiology of IC/BPS, particularly due to the involvement of the urogenital sinus derivatives. Genitourinary syndrome of menopause (GSM) involves urogenital atrophy, which can be observed during physical examination. Androgens and estrogens are vital to genital tissue structure and function [ 49 ]. Given this embryological connection, it is not surprising that changes in hormone levels can influence pain perception. It is therefore reasonable to consider a trial of hormonal therapy even in premenopausal patients [ 50 ].

Clinicians must recognize that gynecologic findings play a crucial, yet complex, role in the diagnosis and management of IC/BPS. Rather than viewing these findings as isolated or secondary, it is important to consider how gynecologic conditions can either coexist with IC/BPS and contribute to or exacerbate its symptoms. Awareness and thorough understanding of these interconnected conditions allows clinicians to address each of the possible sources of pain. While not exhaustive, this narrative review highlights the most prevalent IC/BPS gynecologic co‐morbidities, supported by current literature. Clinical evaluation should prioritize meticulous history‐taking, a careful, trauma‐informed pelvic examination, to establish the role of each overlapping condition. By integrating gynecologic findings into the diagnostic and therapeutic process, clinicians can better manage the multifactorial nature of IC/BPS and improve outcomes for patients. Future directions include developing a multidisciplinary diagnostic and treatment algorithm to guide clinicians—including urologists, gynecologists, urogynecologists, physical therapists—in comprehensive IC/BPS care.

Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is a chronic condition characterized by pelvic pain perceived to be related to the urinary bladder, often accompanied by lower urinary tract symptoms, without an identifiable cause. According to the Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction (SUFU), IC/BPS is defined as “an unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder, associated with lower urinary tract symptoms of more than 6 weeks duration, in the absence of infection or other identifiable causes.” [ 1 ] Despite recent recommendations by the International Urogynecological Association (IUGA) and the American Urogynecologic Society (AUGS) to adopt the term “Female Bladder Pain Syndrome (FBPS)” as a replacement for IC/BPS, this consensus will use the IC/BPS terminology originated by the International Society for the Study of Bladder Pain Syndrome, reflecting its established utilization across urologic and multidisciplinary care settings [ 2 , 3 ]. IC/BPS is a common cause of chronic pelvic pain (CPP) and should be considered in the differential diagnosis [ 4 ]. CPP affects approximately 26% of reproductive‐aged individuals assigned female at birth [ 5 ]. A number of gynecologic disorders may overlap with IC/BPS or be mistaken for it, necessitating careful differentiation. This consensus aims to evaluate the role of gynecologic comorbidities in IC/BPS by reviewing current medical literature and identifying the most relevant gynecologic co‐morbidities.

The authors declare no conflicts of interest.

This consensus statement followed a four‐phase process: Phase 1 : A systematic literature review (inception–January 2025) was conducted across PubMed/MEDLINE, Embase, Cochrane Library, and Web of Science using predefined search terms related to IC/BPS and gynecologic conditions. Sources included: Professional societies : International Society for the Study of Bladder Pain Syndrome, International Urogynecological Association, American Urogynecologic Society, International Society for the Study of Vulvovaginal Disease, International Society for the Study of Women's Sexual Health, and International Pelvic Pain Society. Diagnostic systems and research networks : DSM‐V, ICD‐11, the 4th International Consultation on Sexual Medicine classification system, and the MAPP Research Network. Guidelines and taxonomy references : European Association of Urology Guidelines on Chronic Pelvic Pain, International Continence Society report on chronic pelvic pain terminology, and the International Association for the Study of Pain taxonomy. Professional societies : International Society for the Study of Bladder Pain Syndrome, International Urogynecological Association, American Urogynecologic Society, International Society for the Study of Vulvovaginal Disease, International Society for the Study of Women's Sexual Health, and International Pelvic Pain Society. Diagnostic systems and research networks : DSM‐V, ICD‐11, the 4th International Consultation on Sexual Medicine classification system, and the MAPP Research Network. Guidelines and taxonomy references : European Association of Urology Guidelines on Chronic Pelvic Pain, International Continence Society report on chronic pelvic pain terminology, and the International Association for the Study of Pain taxonomy. Phase 2 : A multidisciplinary panel of six experts (urologists, urogynecologists, gynecologists, pain specialists) was assembled. Phase 3 : Consensus was developed using a modified Delphi method, with multiple electronic rounds and final presentation and discussion at the Global Consensus on IC/BPS (Winston‐Salem, NC; April 23–24, 2025). Phase 4 : Final consensus was refined through iterative manuscript review.